Ren et al. [130] found that CD82 regulates CTCL proliferation and apoptosis through the JAK/STAT and AKT/PI3K pathways and revealed the therapeutic potential of targeting CD82 and JAK, which endow malignant CTCL cells with survival and proliferation advantages. This evidence concerns the gene SOAT1 and primary cutaneous T-cell non-Hodgkin lymphoma.